Project Summary Recent research shows that sleep could play a novel role in preventing obesity and long-term morbidity. Population studies find that too little sleep predicts the development of obesity and experimental studies show that short sleep increases dietary intake without increasing physical activity. Sleep may be a particularly potent intervention target for adolescents. During adolescence, inadequate sleep is very common, obesity rates are rising most, non-sleep-oriented obesity prevention programs have had least success, and young people can develop enduring dietary patterns that set the stage for life-long obesity and health risk. Our lab has shown both the promise of longer sleep for adolescents and a critical knowledge gap. We found that extending adolescents? sleep via earlier bedtimes impressively reduced caloric intake for early chronotypes (?Morning Larks?; who prefer early bed- and rise times), but not late chronotypes (?Night Owls?; who prefer late bed- and rise times). The effect was not only statistically strong, but at roughly 400 calories difference per day, could add up to major shifts in body weight over time. Beyond calorie counts, there was a similar discrepancy in the glycemic load consumed by Larks and Owls after sleep extension, and glycemic load has been independently linked to long-term morbidity. We assert that the discrepancy in how Larks and Owls responded to longer sleep is due to circadian misalignment: a mismatch between the timing of external sleep-wake demands and internal biological clock. We propose that, for adolescent Owls, an early-to-bed intervention induces misaligned sleep timing that counters the benefits of longer sleep duration. In adults, severe circadian misalignment dramatically increases the risk for obesity, and even modest misalignment is linked to higher caloric intake. If a cause-effect relationship holds in adolescence, common sleep advice emphasizing earlier bedtimes might waste limited resources or even do harm for Owls. In contrast, an approach that considers chronotype might capitalize on the potent effect of improved sleep that we have shown for Larks. Here, we propose a novel experimental study in which 124 healthy 14- 18-year-olds (62 Owls and 62 Larks) complete a 3-week trial involving periods of sleep restriction and sleep extension, in which the extension periods are randomly assigned to be aligned vs. misaligned relative to chronotype. Focusing independently on caloric intake and glycemic load, we will assess the dietary effect of sleep extension when it is well-timed versus poorly-timed relative to adolescents? internal clocks. We will test a causal model in which sleep timing plays an important role in promoting or negating the benefits of sleep extension. This is pivotal next step for our research program, which has shown the promise of sleep extension to prevent obesity and morbidity, but so far only for early chronotypes (Larks). At the end of this study, we anticipate having the knowledge needed to better harness the power of sleep to prevent obesity and long-term morbidity for at-risk youth, laying the foundation for more effective public health interventions.